Plasmodium chabaudi adami in C3HeB/FeJ and C57BL/6 mice does not induce a significant malaria-specific IgG1 response during a primary infection. This effect does not appear to be due to the fact that parasite antigens are unable to stimulate an IgG1 response, since those antigens shared with another rodent malaria, P. yoelii, when presented on P. yoelii parasites do induce IgG1 antibodies. Further, a second infection with P. chabaudi will induce a specific IgG1 response. The polyclonal B cell response is similar in its isotypic distribution to that of the malaria-specific response, in that IgG1-secreting cells are only a very minor component of the total response. Infection with P. chabaudi also affects the plaque-forming cell response to sheep erythrocytes. Although the total response is relatively unaffected by infection, the IgG1 response is depressed. IgM, IgG2a, IgG2b and IgG3 are unaltered or enhanced. The mechanism of the IgG1 regulation in this infection is currently under investigation.